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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The incidence, mortality, physiology, clinical findings and diagnosis of phaeochromocytoma are reviewed. Treatment, after adequate medical stabilization, must be surgical because of the high incidence of malignancy. Alpha-adrenergic receptor blockade and beta-adrenergic receptor blockade in the preoperative period was discussed. Anaesthetic management of patients with phaeochromocytoma requires close monitoring. Virtually all inhalational anaesthetic agents have been used in cases of phaeochromocytoma. Recent reports have favored enflurane. The merits of neuroleptanaesthesia and the various muscle relaxants are also discussed. Most authors favour lidocaine over propranolol for management of dysrhythmias during operation. Phentolamine or sodium nitroprusside are used for hypertension during operation. Hypotension is treated by fluid replacement with nor-epinephrine if a vasopressor becomes necessary. Close monitoring is necessary in the postoperative period. Adequate urinary output is of more importance than actual blood pressure levels.
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PMID:Anaesthetic management of phaeochromocytoma. 4 26

This study was designed to investigate whether the cholinergic system is involved in the genesis of the reflex vasodilatation which follows the systemic hypertension induced by fast intravenous injection of norepinephrine in the dog. Accordingly, in 7 dogs the gracilis muscle was isolated and perfused and the reflex evoked. The analysis of the integrated areas of vasodilatation after atropine pretreatment showed a significant decrease of the reflex response in the perfused circulation. In fact, the mean value of the integrated areas of vasodilatation which was 66 +/- 8 mm Hg/min in the control condition, was reduced to 45 +/- 4 mm Hg/min after administration of atropine in the gracilis artery; meanwhile the integrated areas of systemic hypertension did not show any change. Phentolamine intra-arterial administration completely abolished the reflex. These results suggest the existence of a cholinergic component in the reflex vasodilatation induced by transitory baroreceptorial stimulation.
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PMID:Studies on the mechanism of reflex vasodilatation. The cholinergic component in the baroreceptorial reflex in the dog. 61 58

Phentolamine, dihydroergocristine and isoxsuprine were compared for their effects on the blood pressure in anaesthetized normotensive rats, in rats made hypotensive by ganglionic blockade or by pithing and in rats with noradrenaline-induced hypertension. Their ability to inhibit pressor responses elicited by electrical stimulation of the posterior hypothalamus and of the sympathetic outflow from the spinal cord was also investigated. All three drugs appeared very potent in inhibiting noradrenaline-induced hypertension and caused a dose-dependent fall in blood pressure in normotensive rats, which however was less pronounced with dihydroergocristine than with phentolamine and isoxsuprine. In hypotensive rats, dihydroergocristine caused a rise in blood pressure. At higher doses than those required to block noradrenaline-induced hypertension, the three drugs inhibited pressor responses elicited by electrical stimulation and were equally active on peripherally- and centrally-evoked responses. Simultaneous recording of heart rate and blood pressure, both in anaesthetized and in pithed rats, indicated a reflex origin for phentolamine-induced tachycardia and a direct cardiac stimulation for isoxsuprine. Reflex changes of heart rate were not observed with dihydroergocristine.
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PMID:Effects of phentolamine, dihydroergocristine and isoxsuprine on the blood pressure and heart rate in normotensive, hypotensive and hypertensive rats. 81 97

Phentolamine (Regitine) at the dose of 0.3 mg/mn behaves as an arterial and, above all venous, vasodilatator agent, resulting in a marked and early lowering of the pulmonary pressures in acute oedema of the lung and in cardiac asthma. It was used alone in 47 attacks of acute severe left ventricular failure with very favourable results in 43 cases, as proved by the rapid improvement of the haemodynamic status and of the aicd-base balance. Under strict observation, tolerance has been excellent. This therapeutic method seems of great interest in the cases of acute pulmonary oedema with a maintained blood pressure level, and in the forms with severe arterial hypertension which might tolerate larger doses.
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PMID:[Phentolamine in treatment of acute left ventricular insufficiancies]. 81 43

Acute hypertension in rats was produced by intravenous infusion of metaraminol bitartrate (Aramine). The permeability to intravenously injected horseradish peroxidase (HRP) was increased across the cerebral arterioles, capillaries and venules. From the basement membranes of the vessel walls the protein tracer moved into the extracellular spaces of the adjacent neuropil. No endothelial cell damage was observed. The tight junctions between endothelial cells were intact and prevented intercellular movement of peroxidase. Many HRP-labeled vesicles within the endothelial cells or connected with the luminal or abluminal surface, occurred in segments of the microvasculature. Otherwise the endothelium was unchanged. Diffuse uptake of HRP into the cytoplasm of neurons and glial cells was not observed. The alphablocker phentolamine (Regitin) was given to a group of rats simultaneously to Aramine. The increase in blood pressure was thus prevented; furthermore, the permeability remained as under normal conditions. The Aramine, Regitin and HRP did not significantly influence the pH, PO2 and pCO2 of the arterial blood. It is concluded that acute hypertension increases the vesicular transport of HRP across the endothelium of cerebral arterioles, venules and capillaries that normally occurs to a small extent only after intravenous injection of the tracer.
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PMID:Increased vesicular transfer of horseradish peroxidase across cerebral endothelium, evoked by acute hypertension. 84 78

A cardiogenic hypertensive chemoreflex was studied in 38 anesthetized and three unanesthetized dogs. Serotonin (100 mug/ml) injected into either the left atrium or small brancehes of the proximal left coronary artery produced a maximal response, with 96 +/- 18 mm Hg increment in mean aortic pressure within 6 +/- 2 seconds, lasting about 1 min; a later phase of the same hypertension lasted 9 +/- 5 minutes more and could partially be produced with serotonin injected into the thoracic aorta. Injections into the distal left coronary artery produced only the Bezold-Jarisch reflex. Concomitant with the immediate hypertension there were vagal and sympathetic efferent effects in both the sinus node and the atrioventricular (A-V) junction. Either of these effects could be selectively eliminated and the other augmented by direct local perfusion with an appropriate cholinergic (atropine 10 mug/ml) or adrenergic beta-receptor (propranolol 10 mug/ml) blocking agent. Bilateral vagotomy markedly attenuated but did not eliminate the acute hypertension, but it abolished both chronotropic and dromotropic effects. Phentolamine (2 mg/min i.v.) markedly diminished the hypertensive response. Guanethidine or reserpine pretreatment markedly diminished the hypertensive response; reserpine eliminated the electrophsiologic effects but guanethidine did not. Infiltration of serotonin around the main left coronary partially reproduced the reflex, but similar infiltration of xylocaine hydrochloride blocked the reflex. Serial section histologic studies of the region around the main left coronary atery in seven dog hearts and nine human hearts demonstrated the presence of a small structure resembling a chemoreceptor; its blood supply originated from the left coronary artery. Some possible clinical implications are discussed.
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PMID:Analysis of components in a cardiogenic hypertensive chemoreflex. 114 1

The relation of renin-angiotensin status to general hemodynamics and to neurogenic vascular resistance was studied in patients with border-line hypertension. Plasma renin activity during standing was referred to a standard renin-urinary sodium nomogram derived from 18 normal subjects. Among 22 patients with borderline hypertension the renin level was high in 8, low in 4 and within normal limits in the remaining 10. In patients with borderline hypertension and high or normal levels of plasma renin activity, the blood pressure elevation was due to increased total peripheral vascular resistance. In contrast, in patients with low renin borderline hypertension, total peripheral resistance was not significantly elevated; the blood pressure elevation reflected a cardiac index 12 percent higher than that in normal subjects. The neurogenic contribution to total peripheral vascular resistance was assessed by studying the effects of alpha adrenergic blockade with phentolamine, after prior autonomic blockade of the heart with atropine (0.04 mg/kg body weight) and propranolol (0.2 mg/kg). Phentolamine (15 mg) produced an immediate reduction in total peripheral resistance of 12.0 +/- 6.7 percent in patients with high renin borderline hypertension (P less than 0.01) but no change in normal subjects or those with borderline hypertension and normal or low renin levels. Normalization of the blood pressure followed "total" autonomic blockade with atropine, propranolol or phentolamine only in patients with high renin borderline hypertension. It is concluded from these preliminary data that in high renin borderline hypertension the blood pressure elevation is sustained by neurogenic mechanisms. The elevated renin level in these patients is probably an expression of increased sympathetic nervous activity. Although the elevated plasma renin level may possibly be contributing to the generation of higher sympathetic tone, or data do not support a direct role of circulating angiotensin in the maintenance of the elevated vascular resistance.
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PMID:Relation of renin status to neurogenic vascular resistance in borderline hypertension. 119 91

Neuroblastoma is the most common solid tumour in infancy and childhood. The tumour usually produces large amounts of catecholamines. Few patients with neuroblastoma, however, were reported to have become hypertensive because of catecholamine metabolism within the tumour itself. This is one of the most important differences compared with pheochromocytomas. We experienced a hypertensive crisis accompanied by tachycardia and an increase in the plasma catecholamine concentration during surgery in a patient with neuroblastoma. The plasma catecholamine level was comparable to that of pheochromocytoma. Phentolamine and propranolol were effective to control the hypertension and tachycardia.
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PMID:[A hypertensive crisis during surgery in a patient with neuroblastoma]. 157 28

In anaesthetized rats, ventilatory stimulation induced by phentolamine, an alpha sympatholytic agent, emphasizes the role of some adrenergic mechanisms in the control of the respiratory centres activity. Phentolamine (5 and 10 mg.kg-1, iv) stimulates ventilation after a 4 s latency, tidal volume and respiratory rate being both increased. A same response can also be provoked 10 min later, by a second identical iv administration, systemic blood pressure remaining then stable at its previous low level. Hyperventilation is also observed when phentolamine is injected in totally denervated rats, without any remaining baro- or chemosensitivity. Stimulation is thus due to a central activity in relation with the release of inhibitory influences. Phentolamine also causes hyperventilation after prazosin pretreatment indicating that the alpha 1 adrenergic blockade is not involved in the post-phentolamine stimulation. This is an alpha 2 adrenergic transmission dependent mechanism. Variation of the systemic blood pressure is not the main mechanism involved in the hyperventilation induced by phentolamine. Meanwhile, baroreceptor activity modulates the central response to the drug, as shown by the negative influence of the post-vasopressin arterial hypertension. Hyperoxia is also a modulating factor acting by two ways: an inhibition of the peripheral chemoreceptors activity is added to an arterial hypertension. On the other side, activation of these chemoreceptors by almitrine bismesilate increases the respiratory responses to phentolamine. As already shown by one of us (Lagneuax, 1986), phentolamine pretreated rats are more responsive to hypoxia and to almitrine. Moreover, these phentolamine pretreated rats are protected against cardiovascular collapses and against apnea, frequently observed during hypoxia without CO2 compensation.
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PMID:[Alpha 2 adrenergic control of ventilation in the rat]. 170 84

Direct effects of dopamine on renin release were examined using static incubations and perifusions of rat renal cortical slices. Dopamine (10(-5)M) significantly stimulated renin release compared with control. To determine which receptors are involved in dopamine-elicited renin release, studies were performed with specific dopamine-1 and dopamine-2 receptor agonists and antagonists, as well as with alpha- and beta-adrenergic antagonists. Fenoldopam, a dopamine-1 receptor agonist, dose dependently stimulated renin secretion both in static incubations and perifusions; whereas quinpirole (10(-7)-10(-5)M), a dopamine-2 receptor agonist, was ineffective. Phentolamine (10(-4)M), an alpha-adrenergic antagonist, did not alter dopamine- or fenoldopam-induced renin release. Similarly, propranolol, a beta-blocker, did not interfere with the renin stimulation of dopamine (10(-5)M) or fenoldopam (10(-6)M) incubations or perifusion experiments; whereas propranolol significantly blocked isoproterenol action. SCH 23390 (10(-5)M), a specific dopamine-1 antagonist, blocked dopamine- and fenoldopam-induced renin. In contrast, pimozide, a dopamine-2 receptor antagonist, was ineffective. These studies indicate that dopamine is a direct renin secretogogue, and its effects seem to be mediated by specific dopamine-1 receptor activation, as neither alpha- nor beta-adrenergic blockers nor dopamine-2 receptor antagonists altered dopamine actions. The results suggest that dopamine produced locally in the kidney may stimulate renin secretion directly by dopamine-1 receptor activation.
Hypertension 1989 May
PMID:Evidence that specific dopamine-1 receptor activation is involved in dopamine-induced renin release. 256 77


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